Relationship between plasma volume and plasma flow, in the toad.
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Plasma volume was decreased by prolonged bicycle exercise, by passive heating in warm water, by sauna dehydration, and by diuretically induced dehydration in eleven well trained subjects. Blood samples from an arm vein were taken before and after this pre-treatment, as well as after a subsequent standard exercise test (SET) on a bicycle ergometer (50%, 70% and 105% of max VO2; the SET with no pre-treatment was used as a control condition. The changes in plasma concentration of Na+, K+ and Cl- were not proportional to the calculated plasma volume changes. The Na+ and Cl- concentrations always increased in the plasma, while plasma potassium concentration was increased after prolonged exercise, but decreased after the other types of dehydrations. The standard exercise test produced a pronounced fall in total calculated plasma potassium and in K+ concentration measured 3-5 min after exercise in all types of experiments. In the standard exercise test the calculated water loss from the plasma volume was relatively large. It amounted to about 2/3 of the total water loss in the standard exercise test and was independent of the pre-treatments.
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Six stable chronic hemodialysis patients received six hemodialysis treatments: two each with the dialysate sodium concentration (DNa) 7% greater than serum sodium concentration, two with a DNa equal to serum sodium concentration and two with the DNa 7% less than the serum sodium concentration. During one treatment with each dialysate 2 kg of fluid was removed and during the other treatments the patient's weight was kept constant. Total body water (TBW), intracellular water (ICW), extracellular water (ECW), plasma volume (PV), plasma renin activity (PRA), aldosterone (ALDO), Na, BUN and osmolality were determined before and after each treatment. Fluid removal during dialysis had no effect on ICW with essentially all the fluid removed during dialysis coming from ECW. ICW increased with low DNa and decreased with high DNa. The effect of DNa on ECW and PV was the opposite of that on ICW. PRA increased and ALDO decreased during dialysis. Predialysis ALDO directly correlated with PRA (r = 0.68, p less than 0.001) but not with serum potassium concentration. Post dialysis ALDO was not significantly correlated with either PRA or potassium. Fluid removal and low DNa increased both PRA and ALDO. These studies indicate that water shifts from the extracellular space into intracellular space when DNa is lower than serum Na and the reverse is true when DNa exceeds serum Na. Plasma aldosterone decreases during dialysis despite an increase in PRA, possibly related to the decrease in serum potassium concentration. The effect of fluid removal and low DNa on PRA and ALDO may be related to a reduction in ECW and/or PV.
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The effect of alterations in serum protein levels on plasma volume in tropical splenomegaly syndrome has been investigated by determining plasma volume, serum albumin, globulin and immunoglobulin levels in 64 adult New Guineans suffering from this disease. Plasma volumes ranged from 51-2 to 129 ml./kg. Significant positive correlations were found between plasma volume and intravascular pools of albumin, IgG and IgM. Multiple regression analysis demonstrated that 70% of the variance in plasma volume in this series was attributable to increases in these three pools, IgM and IgG accounting for 42% of the total and albumin for 28%. It is probable that the unexplained 30% of plasma volume expansion arises through a splenic arterio-venous shunt effect. It is suggested that initially in tropical splenomegaly syndrome the splenic shunt and immunoglobulin overproduction combine to produce expansion of plasma volume and a fall in intravascular colloid osmotic pressure; that the latter provides the stimulus to increased albumin synthesis, and that this further aggravates the plasma volume expansion and the consequent dilutional anaemia commonly seen in this disease.
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OBJECTIVE: This study aimed to test the hypothesis that the initial distribution volume of glucose (IDVG) is correlated with plasma volume determined by indocyanine green (ICG) following colloidal fluid challenges. The IDVG was also compared with cardiac output (CO) as measured by the conventional thermodilution method. DESIGN AND SETTING: The study was prospective and was conducted in the animal laboratory, University of Hirosaki School of Medicine, after approval of the institutional animal experiment committee. PARTICIPANTS: Thirteen mongrel dogs of either sex, weighing 9.0-14.5 kg, were the subjects of the study. INTERVENTIONS: They were anesthetized with pentobarbital and paralyzed with pancuronium. 30 ml x kg(-1) of 3% dextran in lactated Ringer's solution was given twice to induce a hypervolemic state. MEASUREMENTS AND RESULTS: In each stage of the fluid loading, the IDVG, plasma volume and CO were measured simultaneously. The IDVG was measured following an injection of glucose (100 mg x kg(-1)) by repeated determinations of plasma glucose (3-7 min) with a one-compartment model, and plasma volume was assessed similarly following ICG (0.5 mg x kg(-1) injection. A closer correlation was observed between the IDVG and plasma volume (r = 0.79, p < 0.001) than between the IDVG and CO (r = 0.48, p < 0.01). CONCLUSION: The IDVG correlates with plasma volume following volume challenge in dogs. CO did not show a consistent change following volume challenge. The IDVG may have the potential as an indicator to presume the fluid volume in the body, even though the IDVG cannot be used directly to estimate plasma volume.
To test the hypothesis that the initial distribution volume of glucose (IDVG) reflects plasma volume, the relationship between the IDVG and indocyanine green (ICG) assessments of plasma volume (Vd-ICG) were evaluated simultaneously both before and after induced haemorrhage (30 ml.kg-1) in eight mongrel dogs. The IDVG and the Vd-ICG were calculated with a one-compartment model from repeated measurements of plasma glucose three to seven minutes, and of plasma ICG three to nine minutes after simultaneous infusions of both glucose 100 mg.kg-1 and ICG 0.5 mg.kg-1. The IDVG calculated with a one-compartment model (IDVG-OCM) was also compared with a two-compartment model within 15 min (IDVG-TCM) on nine occasions among a total of 12 determinations. Using Bland and Altman analysis to compare the two analytical models, the IDVG-OCM tends to overestimate the IDVG-TCM by an average of 0.04 L. Although the IDVG-OCM was two to three times larger than the Vd-ICG at each corresponding point, a correlation was obtained between the IDVG-OCM and the Vd-ICG before and after induced haemorrhage (r = 0.85, n = 16, P < 0.001). We conclude that the IDVG reflects plasma volume in normal and hypovolaemic dogs, although the IDVG cannot be used directly to estimate plasma volume.
Plasma antidiuretic hormone (ADH) was measured before and after furosemide administration in hypertensive patients (essential benign hypertensions with low plasma renin activity) and in normal subjects. Furosemide-induced reduction of plasma volume was about 10% after 2 hours. In normal subjects, plasma ADH rose progressively till the end of the study (1.5 pg/ml per hour corresponding to about 3 pg/ml per liter of plasma water lost) whereas it remained unchanged in hypertensive patients. There was an early increase of plasma renin activity (PRA) in normal subjects followed by a progressive fall. PRA response was blunted in hypertensive patients. These results show that volume-dependent ADH secretion is inhibited in patients with essential benign hypertension.
Plasma volume expanders are effective in the restoration of blood volume. All the available plasma volume expanders may rarely induce anaphylactoid reactions, although such reactions are extremely uncommon in shocked patients. The reactions are caused by different mechanisms depending on the solution, and there is little evidence that IgE antibodies are involved. In addition to these reactions, effects on haemostasis and renal function may occur, and the persistence of hydroxyethyl starch in the body has led to concern about its potential role as a carcinogen, although there is no evidence to suggest that this has occurred.
Conscious, intact and splenectomized, male dogs were hemorrhaged 35 percent of their blood volumes (23 +/- 3 and 25 +/- 4 ml/kg, respectively) from carotid loop cannulas. Isotonic saline or glucose solutions were administered by gastric tube in volumes equal to the blood volume hemorrhaged. Plasma volume, mean arterial blood pressure, venous hematocrit, plasma protein concentration, and interstitial fluid pressure were monitored after hemorrhage and after fluid treatment. The magnitudes of plasma volume restoration 8 h after hemorrhage in the nontreated dogs averaged 56 +/- 9 percent of the hemorrhaged volume and did not differ significantly between intact and splenectomized dogs. Plasma volumes, however, were increased significantly by enterally administered fluids. The maximum rates of plasma volume restoration occurred within the 1st h after fluid treatment. Approximately 46 percent and 28 percent of the hemorrhaged plasma volume was replaced by saline and glucose solutions, respectively, during this period. Results support the hypothesis that fluid is absorbed from the gastrointestinal tract following hemorrhage, and that enterally administered fluids restore plasma volume at a rate and to an extent exceeding that provided by net interstitial fluid exchange alone.
Little is known about mechanisms of systemic hypotension frequently reported during plasma exchange (PE). Type of substitution fluids may interfere with hemodynamic tolerance. In a prospective study, right heart catheterization was performed during 18 PE by filtration with isovolumic substitution. Blood volume was measured with 51Cr tagged erythrocytes and plasma volume (PV) calculated from hematocrit. Substitution fluids were either albumin (A; n = 9) or A + gelatin (A + G; n = 9). In both groups, PE induces significant (p less than 0.01) decreases of mean arterial pressure: group A: - 21 +/- 14%; group A + G: - 23 +/- 15%; of pulmonary wedge pressure: group A: - 41 +/- 33%; group A + G: - 36 +/- 22%; of cardiac index: group A: - 38 +/- 18%; group A + G: - 25 +/- 15%. Plasma volume also decreases after PE: group A: - 13.5 +/- 4%; group A + G: - 18.5 +/- 4%. None of the variations are significantly different between the two groups. So we think that substitution with albumin alone has no advantage for hemodynamic tolerance.
Five different experiments were conducted to determine if estimated liver plasma flow and/or plasma volume were changed as a result of exposure to 2.8 atmospheres absolute (ATA) while breathing 100% oxygen or 6 ATA while breathing compressed air. The experiments were designed to separate the relative roles of the ambient pressure, the partial pressure of oxygen, the time of high oxygen exposure or some combination of these factors on any observed changes. We found that time was not a factor in the changes seen. Hyperbaria resulted in a decrease in estimated liver plasma flow at all pressures greater than 1 ATA. There was an apparent increase in plasma volume at 1.3 ATA and a return towards 1 ATA values at higher pressures. Hyperoxia resulted in a decrease in estimated liver plasma flow at 975 mm Hg but not at 912 mm Hg. The flow was then increased again at 2128 mm Hg. Plasma volume decreased significantly at 912 mm Hg returned to baseline (152 mm Hg) values at 975 mm Hg and then decreased again at 1054 and 2128 mm Hg PO2.
BACKGROUND: To compare plasma lactate concentrations and plasma lactate kinetics during recovery, for measured and corrected values for changes in plasma volume, after a maximal aerobic exercise. METHODS: Sixteen male subjects performed an incremental and maximal exercise in order to reach maximal aerobic power. Prior to the exercise, at the end and during recovery (2, 5, 12 and 30 min), blood samples were collected through an antecubital catheter. Samples were analysed for lactate, hematocrit and hemoglobin in order to calculate changes in plasma volume. Plasma lactate concentrations ([La]p) were corrected for changes in plasma volume. Plasma lactate kinetics was estimated through the ratio between [La]p after 5 min recovery minus [La]p after 30 min to time (25 min) and expressed in percentage per minute. RESULTS: Maximal changes in plasma volume (-19.7 +/- 3.8%) were correlated to maximal measured [La]p (r=0.66, p<0.01). Maximal measured [La]p values (14.9 +/- 2.6 mmol x l-1) were 17.3% higher (p<0.001) than corrected values (12.7 +/-2.0 mmol x l-1). The kinetics of [La]p decrease was significantly higher (p<0.001) for measured values (2.38 +/- 0.29 % x min-1) than for corrected values (2.22 +/- 0.33 % x min-1). CONCLUSIONS: These results suggested that changes in plasma volume must be taken into account when peak postexercise plasma lactate concentration or lactate recovery curves are analysed.
Changes in hematocrit and plasma oncotic pressure were measured continuously during and after isotonic volume expansion in splenectomized dogs in order to test the potential of these types of measurements to predict changes in plasma volume. A volume of Ringer's solution amounting to 15% of the initial blood volume was infused over 10 min. At the end of the infusion, 54% of infused fluid remained within the intravascular space and 9% of the infused volume was retained within the intravascular space at 50 min after the end of the infusion. Hematocrit and plasma oncotic pressure decreased by 2.4% and 2.4 mmHg, respectively, at the end of infusion and then variables returned to their control levels gradually. Changes in plasma volume were estimated indirectly from hematocrit and plasma oncotic pressure based on the dilution of the erythrocytes and the protein. Highly significant correlations were observed between the measured plasma volume (Y) and the plasma volume (X) calculated from hematocrit (Y = 0.95X + 0.22, r = 0.96) and the plasma oncotic pressure (Y = 0.86X + 0.46, r = 0.91). We therefore conclude that either hematocrit and plasma oncotic pressure measured continuously are reliable parameters for predicting the time course of the plasma volume change during an isotonic volume expansion of up to 15% of the initial blood volume.
Our purpose was to determine the plasma-volume (PV) change induced by a physical stress independent of the metabolic events that may interfere with physiological fluid shifts in to and out of the intravascular space. Our methods included using 178 exercise tests of varying duration and intensity for determination of PV change during exercise. Plasma Fourier transform infrared (FT-IR) spectra were used to compare hematocrit change to the total spectral area (4000-500 cm(-1)) and the protein and albumin concentration changes induced by exercise. Our results showed that exercise induced a raise in protein (+10.4 +/- 3.1%) and albumin (+9.8 +/- 3.3%) concentrations that significantly correlated with PV change (14.1 +/- 5.2% of plasma volume; P = 0.05 with protein and albumin concentration changes). However, evolution of the total spectral area obtained from rest-plasma (524 +/- 21 a.u.) and exercise-plasma (611 +/- 26 a.u.; +14.1 +/- 4.8%) FT-IR spectra showed a higher correlation level with PV change (r = 0.98; P = 0.005; S(x/y) = 1.26 a.u.). It is our conclusion that although exercise-induced changes in protein and albumin concentrations were found to correlate with PV change, the use of the total spectral area of the plasma FT-IR spectra allowed a more precise measurement of PV change.
Microelectrode recordings of muscle nerve sympathetic activity and measurements of venous plasma noradrenaline have indicated increased sympathetic outflow during acute hypoglycaemia. Plasma volume reduction during hypoglycaemia, as evidenced by increasing peripheral venous haematocrit might underly the sympathetic activation. To study the effect of prevention of plasma volume reduction during hypoglycaemia, saline containing albumin was infused intravenously in healthy adult volunteers during hypoglycaemia. Hypoglycaemia was induced by an intravenous injection of soluble insulin in a dose of 0.15 IU/kg body weight. Peripheral venous plasma noradrenaline concentrations were identical in experiments without and with plasma volume substitution. Muscle nerve sympathetic activity increased to the same extent during hypoglycaemia with and without plasma volume substitution. It is concluded that increased plasma noradrenaline concentrations and enhanced muscle nerve sympathetic activity during insulin-induced hypoglycaemia in man are not consequences of plasma volume reduction.